"Sarcolemma" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
The excitable plasma membrane of a muscle cell. (Glick, Glossary of Biochemistry and Molecular Biology, 1990)
Below are MeSH descriptors whose meaning is more general than "Sarcolemma".
Below are MeSH descriptors whose meaning is more specific than "Sarcolemma".
This graph shows the total number of publications written about "Sarcolemma" by people in this website by year, and whether "Sarcolemma" was a major or minor topic of these publications.
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|Year||Major Topic||Minor Topic||Total|
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Below are the most recent publications written about "Sarcolemma" by people in Profiles.
A gene-edited mouse model of limb-girdle muscular dystrophy 2C for testing exon skipping. Dis Model Mech. 2019 11 04; 13(2).
Genetic modifiers of muscular dystrophy act on sarcolemmal resealing and recovery from injury. PLoS Genet. 2017 Oct; 13(10):e1007070.
Intermittent glucocorticoid steroid dosing enhances muscle repair without eliciting muscle atrophy. J Clin Invest. 2017 Jun 01; 127(6):2418-2432.
Cholesterol depletion impairs contractile machinery in neonatal rat cardiomyocytes. Sci Rep. 2017 03 03; 7:43764.
An actin-dependent annexin complex mediates plasma membrane repair in muscle. J Cell Biol. 2016 06 20; 213(6):705-18.
Enhanced Muscular Dystrophy from Loss of Dysferlin Is Accompanied by Impaired Annexin A6 Translocation after Sarcolemmal Disruption. Am J Pathol. 2016 06; 186(6):1610-22.
Reengineering a transmembrane protein to treat muscular dystrophy using exon skipping. J Clin Invest. 2015 Nov 02; 125(11):4186-95.
Annexin A6 modifies muscular dystrophy by mediating sarcolemmal repair. Proc Natl Acad Sci U S A. 2014 Apr 22; 111(16):6004-9.
EHD1 mediates vesicle trafficking required for normal muscle growth and transverse tubule development. Dev Biol. 2014 Mar 15; 387(2):179-90.
Ultrastructural and cellular basis for the development of abnormal myocardial mechanics during the transition from hypertension to heart failure. Am J Physiol Heart Circ Physiol. 2014 Jan 01; 306(1):H88-100.